This document provides an overview of analgesics, with a focus on non-steroidal anti-inflammatory drugs (NSAIDs). It defines pain and discusses the classification, mechanism of action, and history of analgesics. NSAIDs are introduced as a class of drugs that relieve pain and inflammation by inhibiting cyclooxygenase (COX) enzymes and subsequent prostaglandin synthesis. The document outlines the role of prostaglandins in inflammation and bone resorption, as well as the beneficial and harmful actions of NSAIDs through COX inhibition. Host modulation is discussed as a treatment concept in periodontics where NSAIDs may reduce tissue destruction by modulating the host inflammatory response.

2. ANALGESICS
Non Steroidal Anti-Inflammatory Drugs

3. CONTENTS
• Introduction
• Classification of analgesics
• Mechanism of inflammation
• NSAIDs:
1. Mechanism of action
2. Classification
3. Various drugs and its indication in periodontics
4. Choice of NSAIDs
5. NSAIDs as host modulatory agent
6. Recent advances
• Conclusion
• References

4. INTRODUCTION:
DEFINITION OF PAIN (ALGESIA)
PAIN is an unpleasant sensory and emotional experience
associated with actual or potential tissue damage, or
described in terms of such damage.
The international association for the study of
pain
An unpleasant emotional experience usually limited by
noxious stimulus and transmitted over a specialized
neural network to the CNS where it is interpreted as such.

5. HISTORY
• Derived from Greek word “Poin” meaning “Penalty.”
• Latin word “Poena” meaning “Punishment from God.”
• Homer thought pain was due to arrows shot by God.
• Aristotle who probably the first to distinguish 5 physical
senses considered pain to the “passion of the soul” that
somehow resulted from the intensification of other
sensory experience.

6. RELATED TERMS
• Allodynia
• Hyperalgesia & hypoalgesia
• Hyperesthesia & hypoesthesia
• Hyperpathia
• Causalgia
• Neuralgia

7. INCIDENCE OF PAIN
• According to Cohen: it was found that 21.8% of adult in
the United States experience orofacial pain symptoms
The most common pain was toothache, which was
estimated to have occurred in 12.3% population

8. MANAGEMENT OF PAIN
• Local anaesthetics
• Analgesics
• Conscious sedation

9. ANALGESIC
• Analgesics relieve pain as a symptom, without
affecting its cause.
• Used when the noxious stimulus cannot be removed
or as adjuvants to more etiological approach to pain.
A drug that selectively relieves pain by acting in the CNS
or on peripheral pain by acting in the CNS or on peripheral
pain mechanisms, without significantly altering
consciousness.

10. ANALGESIA SYSTEM
IN BRAIN
• The degree to which a person reacts to pain varies
tremendously.
Endogenous capability of the brain itself to suppress
the input of pain signals to the nervous system by
activating a pain control system, called an Analgesia
System.

11. ANALGESIA
SYSTEM
Periaqueductal gray
& Periventricular
areas
Raphe magnus
nucleus
A pain inhibitory
complexes

12. CLASSIFICATION
ANALGESICS
Opioid/ Narcotic/
Morphine-like
analgesics
Nonopioid/ Non-
narcotic/ Aspirin-like/
Anti-pyretic or Anti-
inflammatory
analgesics

13. NON-OPIOID ANALGESICS
NSAIDs

14. DEFINITION
• The term NSAIDs are chemically diverse class of
drugs (>70 NSAIDs in use) that have anti-
inflammatory, analgesic & antipyretic properties.
• In 1971 John Vane & co-workers made the landmark
observation that Aspirin & some NSAIDs blocked PG
generation.
• This is now considered to be the main MOA of
NSAIDs.

15. HISTORY
• Willow bark (Salix alba): for many centuries
• Salicylic acid hydrolysis of bitter glycoside
• Sodium salicylate: fever & pain, 1875
• Introduction of acetylsalicylic acid (aspirin), 1899
Fredrich Bayer
& Co
• Major advance: phenylbutazone, 1949 having anti-
inflammatory activity comparable to corticosteroids
• Indomethacin, 1963
• Propionic acid derivative, ibuprofen have been added since
then & COX inhibition is recognized to be their MOA.

16. CLASSIFICATION KD Tripathi

17. Prostagla
ndin
Arachidon
ic acid
Leukoteri
neINFLAMMATION COX-1
CyclesCOX-2

18. INFLAMMATION
• The inflammatory response is complex involving
immune system & various endogenous agents like
prostaglandins, bradykinin, histamine, chemotactic
factors & superoxide free radicals formed by the action
of lysosomal enzymes
• PGs, Prostacyclins & TXA2 have been associated with
gingivitis, periodontitis & alveolar bone resorption
Goodson et al, 1974
Williams, 1990

19. MECHANISM OF ACTION IN
INFLAMMATION
Tissue injured
Inflammation
PG, Histamine, Bradykinin, IL-1,
TNF-α etc

20. PROSTAGLANDINS ?
Prostaglandins are lipid autacoids derived from
arachidonic acid.
They both sustain homeostatic functions and mediate
pathogenic mechanisms, including the inflammatory
response. They are generated from arachidonate by the
action of cyclooxygenase (COX) isoenzymes and their
biosynthesis is blocked by nonsteroidal anti-inflammatory
drugs (NSAIDs)

21. ROLE OF PGs IN INFLAMMATION
Prostaglandi
ns have 2
major
actions
•They are mediators of
inflammation
•Sensitize pain receptors at the
nerve endings, lowering their
threshold of response to stimuli &
allowing other mediators of
inflammation

22. ROLE OF PGs IN BONE
RESORPTION
• In number of ways and may induce bone resorption by
facilitating the release of osteoclasts activating factor
from lymphocytes.
Yoneda & Mundy 1979
• Inhibit bone collagen formation which result in
inhibition of the repair of resorbed bone.
Raisz & Koolemans –
Beynen 1974

23. ROLE IN PERIODONTAL DESTRUCTION
Production of arachidonic acid metabolites :
• After activation of inflammatory cells in the
periodontium by bacteria, phospholipids in the plasma
membrane of cells become available for actions by
phospholipase. This leads to free arachidonic acid in the
area.
AAP,
1992

24. Injury/infection/trauma
Attacks the cell membrane of the cell
Cell membrane contains phospholipids
Activation of phospholipase occurs
Formation of arachidonic acid
Cyclooxygenase
pathway
Lipooxygenase
pathway
FORMATION OF ARACHIDONIC ACID

25. CYCLOXYGENASE ENZYMES
(COX)
CYCLOXYGENASE ENZYME (COX)
COX-1 COX-2
• Synthesis of several mediators
• Protects gastric mucosa
• Regulates Renal blood flow
• Initiates platelet aggregation
• Tissue damage such
As pulpitis, periodontitis
Surgery, induce its
production
Synthesis of PGs
Sensitizes pain fibersinflammation
Meade et al.
1993

26. BIOSYNTHESIS OF PROSTAGLANDIN

27. ARACHIDONIC ACID CASCADE

28. NATURALLY, A drug that prevents the synthesis
of prostaglandin is likely to be effective in relieving
pain due to inflammation of any kind

30. MECHANISM OF ACTION OF
NSAIDS

31. BENEFICIAL ACTIONS DUE TO
PGs SYNTHESIS INHIBITION
• Analgesia
• Antipyresis
• Antiinflammatory
• Antithrombotic
• Closure of ductus arteriosus

32. SHARED TOXICITIES DUE TO
PGs SYNTHESIS INHIBITION
Gastric mucosal damage
Bleeding
Limitation of renal blood flow: Na+ & H2O retention
Delay/prolongation of labour
Asthma and anaphylactoid reactions in susceptible
individuals.

33. BENEFICIAL ACTIONS

34. ANALGESIA
• PGs hyperalgesia
• PGs in CNS lowers threshold of pain circuit
• NSAIDs block this pain sensitizing mechanism,
therefore effective against inflammation associated
pain

35. ANTIPYRESIS
• Fever during infection generation of pyrogens (Ils,
TNFα)
• NSAIDs block the action of pyrogens (COX-2)
PGE2 in hypothalamus
Raise its temperature
Set point

36. ANTI-INFLAMMATORY
• Inhibition of PG synthesis at the site of injury
• Anti-inflammatory action of each drug corresponds
with their potency to inhibit COX
• NSAIDs: stabilizes leukocytes lysosomal membrane &
antagonises certain action of kinins

37. DYSMENORRHEA
• Increase level of PGs in menstrual blood flow, endometrial
biopsies & their metabolites is seen in dysmennorhic women
• Mymometrial ischaemia; menstrual cramps
• NSAIDs lowers uterine PG levels excellent
relief (60-70%)

38. ANTIPLATELET AGGREGATORY
• Inhibits synthesis of TXA2 by acetylating platelet
COX, irreversibly
• Inhibit platelet aggregation prolonged bleeding
time
• Small doses are therefore able to exert anti-
thrombotic effect for several days.
• Risk of surgical bleeding is enhanced

39. DUCTUS ARTERIOSUS
CLOSURE
• NSAIDs bring about closure of ductus arteriosus within a
few hours by inhibiting PG production
• PRESCRIBING NSAIDs NEAR TERM SHOULD BE
AVOIDED
Administration of NSAIDs in late pregnancy
promotes premature closure of ductus in some
cases

40. DUCTUS ARTERIOSUS
CLOSURE
• NSAIDs bring about closure of ductus arteriosus within a
few hours by inhibiting PG production
• PRESCRIBING NSAIDs NEAR TERM SHOULD BE
AVOIDED
Administration of NSAIDs in late pregnancy
promotes premature closure of ductus in some
cases

41. NSAID’S AS HOST MODULATORY
AGENTS
• Concept of host modulation was 1st introduced by
Williams, 1990 and Golub et al, 1992
• To modify or reduce destructive aspects of host response:
so that immune-inflammatory response to plaque is less
damaging; host modulation therapies has been developed
• Treatment concept that aims to reduce tissue
destruction and stabilize or even regenerate the
periodontium by modifying or down regulating
destructive aspects of host response and upregulating
protective or regenerative responses
CARRANZA

42. • HMTs are systemically or locally delivered
pharmaceuticals that are prescribed as part of periodontal
therapy and are used as adjuncts to conventional
periodontal treatments
• HMTs do not “switch off” normal defense mechanism or
inflammation; instead, they ameliorate excessive of
pathologically elevated inflammatory processes to enhance
opportunities for wound healing.

43. SYSTEMIC NSAIDs
• Inhibits prostaglandins
• Reduce inflammation
• Used to treat pain, acute inflammation, and chronic
inflammatory conditions.
• Inhibits osteoclastic activity in periodontitis
Howell TH in oral bio med
1993
• NSAIDs such as indomethacin(williams RC 1987)
flurbiprofen (jeffcoat MK JP 1989) and naproxen (Howell TH
1993) administered daily for up to 3 years, significantly
slowed the rate of alveolar bone loss compared with placebo

44. NSAIDS – LOCALLY
ADMINISTERED
• Topical NSAIDs have shown benefit in the treatment of
periodontitis
MATERIAL & METHODS: local drug delivery preparations of a poloxamen gel
containing 1.5% ketoprofen and a placebo were indigenously prepared for this
purpose
CONCLUSION: locally delivered ketoprofen with SRP was more effective in
controlling periodontal disease than SRP alone.

45. One study of 55 patients with chronic periodontitis who received
topical ketorolac mouth rinse reported that GCF level of PGE2
were reduced approximately half over 6 months and that bone loss
was halted
Jeffcoat MK, Reddy MS, Haigh S et al

46. HARMFUL ACTIONS

47. PARTURITION
• Sudden increase in PG synthesis by uterus triggers
labour & facilitate its progression
• NSAIDs: delay & retard labour

48. GASTRIC MUCOSAL DAMAGE
• Gastric pain, mucosal erosion, ulceration & blood loss
are produce by all NSAIDs to varying extent
• Inhibition of COX-1 mediated synthesis of gastro-
protective PGs (PGI2, PGE2)
• Reduces mucus & HCO3- secretions, enhance acid
secretion & promote mucosal ischaemia

49. RENAL EFFECTS
• Conditions like hypovolaemia, decrease renal perfusion,
and Na+ loss renal PG synthesis
vasodilatation, inhibition of Cl – reabsorption
opposing ADH action
• NSAIDs produce renal effects by at least 3 mechanisms:
1. Cox-1 dependent impair renal blood flow, & decrease in
gfr renal insufficiency.
2. JG Cox 2 dependent Na and water retention.

50. ANAPHYLACTOID REACTIONS
• Bronchial asthma, angioneurotic swelling, utricaria
or rhinitis in certain individuals

51. INDICATIONS IN DENTISTRY
• Irreversible pulpitis
• Apical periodontitis
• Acute alveolar abscess
• Infected cyst
• Sinusitis
• TMJ Arthritis
• MPDS
• After tooth extraction
• Dry socket
• Recurrent apthous ulcers
• Lichen planus
• Agranulocytosis
• Cyclic neutropenia

52. SALICYLATES: ASPIRIN
• Acetylsalicylic acid
• Rapidly converted in the body to salicylic acid
• Acetylation of certain macromolecules including
COX
• Oldest analgesic-anti-inflammatory drugs

53. PHARMACOLOGICAL ACTIONS
1. ANALGESIC, ANTIPYRETIC, ANTIINFLAMMATORY
• Aspirin 600 mg = Codeine 60 mg
• Effective in relieving tissue injury related pain but
ineffective in severe visceral & ischaemic pain
• Analgesic action: obtunding of peripheral pain receptors &
prevention of PG mediated sensitization of nerve endings
• Antipyretic action: Resets hypothalamic thermostat &
rapidly reduces fever by heat loss, but doesn’t decrease heat
production
• Antiinflammatory action: (3-6 gm/day or 100mg/kg/day).
Pain, tenderness, swelling, vasodilation & leucocyte
infiltration are suppressed.

54. 2. METABOLIC EFFECT
• Hyperglycemia seen at toxic doses
Central sympathetic stimulation release
Adr & Cortocosteroids
Cellular
metabolism
sed (skeletal
muscles)
Increased
heat
production
Increase
utilization of
glucose
Blood sugar
decrease &
liver glycogen
is depleted

55. 3. RESPIRATION
• Effects are dose dependent
• Antiinlammatory doses: respiration is stimulated by
peripheral & central actions
• Hyperventilation is prominent in salicylate poisoning
• Further rise in level causes respiratory depression
• Death
4. ACID-BASE & ELECTROLYTE BALANCE
• Aspirin produce a state of compensated respiratory
alkalosis (4-5 g/day)
• Higher doses: respiratory acidosis
• Dissociated salicylic acid, metabolic acids + sulphuric
acid, phosphoric acid uncompensated metabolic
acidosis

56. 5. CVS
• Larger doses increase CO to meet peripheral O2
demand vasodilation
• Toxic doses depresses vasomotor centre BP fall
• Increased cardiac work as well as Na+ & H2O retention,
CHF may be precipitated in patients with low cardiac
reserve.
6. GIT
Irritates
gastric mucosa
Epigastric
distress
Nausea &
vomiting
Aspirin particle
Gastric mucosa
Local back diffusion of acid
Focal necrosis of mucosal cells
& capillaries
Acute ulcers, erosive gastritis,
congestion & microscopic
haemorrhages
Occult blood loss in stools is
increased by even a single tablet of
Aspirin

57. 7. URATE EXCRETION
• <2 g/day: urate retention & antagonism of all other
uricosuric drug
• 2-5 g/day: variable effects, often no change
• >5 g/day: increased urate excretion
8. BLOOD
• Irreversibly inhibits TXA2 synthesis by platelets
• Interferes with platelet aggregation
• Bleeding time is prolonged to nearly twice the
normal value
Long term intake of large dose
decreases synthesis of clotting
factors in liver & predisposes to
bleeding

58. ASPIRIN AS ANTIPLATELET
ACTION
PLATELET AGGREGATION PATHWAY

59. Injury
Platelet plug
formation
initiated
Adherence of
Platelet
Subendothelial
collagen
Platelet in
arterial blood
Decrease
velocity
Collagen bound
VWF
Stopped
Binding to the
collagen by GP
receptor complex
Phospholipase
C mediated
cascade
Mobilization of
ca+
Activation
of kinase
Phospholipas
e A2AATXA2
PLATELET
AGGREGATION
COX-1
PGH2
Platele
t
granul
ar
content
ADP+ATP+
Serotonin
Procoagulant
surfaceCoagulation
factor
prothrombinthrombin

60. ASPIRIN
2-3 g/day
-
-
PGI2 (vasodilation,
inhibits platelet
aggregation)
TXA2 (vasoconstriction,
promotes platelet
aggregation)
LOW DOSE ASPIRIN
50-325 mg
-

61. • TXA2 are exposed to aspirin in the portal
circulation. Here, it acetylates COX
enzyme & irreversibly inhibits TXA2. very
little aspirin reaches systemic circulation
to inhibit PGI2 synthesis
• Platelets lack nuclei & cannot synthesize
new COX enzyme once it is inhibited,
whereas endothelium can regenerate COX
enzyme to produce PGI2. Net effect is
thus inhibition of TXA2 generation

62. PHARMACOKINETICS
 Absorption: stomach & small intestine; poor water
solubility
 Deacetylated in gut wall, liver, plasma & other tissues to
release salicylic acid
 80% bound to plasma proteins & has a volume of
distribution of 0.17 L/kg
 Slowly enters brain; freely crosses placenta
 Conjugated in liver with glycine forming salicyluric acid
 Excreted by glomerular filtration as well as tubular
secretion
 Plasma t1/2: 15-20 min; anti-inflammatory doses: 8-

63. ADVERSE EFFECT
 Side effects
 Hypersensitivity & idiosyncracy
 Salicylism : High doses (at antiinflammatory doses) or
chronic use of aspirin may induce a syndrome
characterised by tinnitus, hearing defects, blurring of
vision, dizziness, headache, mental confusion,
hyperventilation and electrolyte imbalance
• Effects are reversible

64. ACUTE SALICYLATE
POISONING
common in children
Fatal dose in adult: 15-30 g
Serious toxicities seen
at serum levels >50mg/dl
MANIFESTATION:
vomiting, dehydration, electrolyte
imbalance, acidotic breathing,
hyper/hypoglycemia, petechial
hemorrhages, restlessness, delirium,
hallucinations, hyperpyrexia,
convulsions, coma and death due to
respiratory and cardiovascular
failure
TREATMENT:
-Symptomatic and
supportive
-external cooling
-Gastric lavage
-I.V. infusion of Na+, K+,
HCO3 and glucose(dextrose-
5%)
-Vitamin K 10mg I.V.
-Peritoneal dialysis or
hemodialysis

65. PRECAUTIONS AND
CONTRAINDICATIONS
• Peptic ulcer
• Sensitive patients
• Children suffering from influenza, chickenpox
• Chronic liver diseases
• Diabetics
• CHF, lower cardiac reserve
• Should be stopped 1 week before elective surgery
• Pregnancy
Delayed labor, more postpartum bleed,
premature closure of ductus arteriosus
• G6PD deficiency

66. USES
1.As analgesic (0.3g-0.6g /day 6-8hrly; max at 1000mg)
2. As antipyretic- in various infections
3. Acute rheumatic fever
4. Rheumatoid arthritis (3-5g/day)
5. Osteoarthritis
6. Postmyocardial infraction & poststroke patients (60-
100mg/day).

67. DOSES
• As analgesic and antipyretic:
 0.3-0.6gm, 6-8 hourly
• Acute rheumatic fever:
 75-100mg/kg/day in divided doses/4-6 days
 50mg/kg/day/2-3wks- maintenance dose
• Rheumatoid arthritis:
 3-5gm/day
• Cardio protective:
 80-100mg/day
Low dose Aspirin: 50-325 mg/day
High dose Aspirin: 2-3 g/day

68. DENTAL CONSIDERATION
BT
CT
PT
INR

69. PERIODONTAL INDICATION
Low-dose aspirin irreversibly inhibits COX over
the whole lifetime of platelets
middle-aged and elderly populations
preventing inflammation, coronary artery
disease, stroke and peripheral vascular diseases
and its lower gastro-intestinal side effects
The powerful inhibitory effects of aspirin on COX metabolites,
including PGE2, has stimulated many studies of the effects of
aspirin and NSAIDs on periodontal diseases
Underwood 1994, Diener 1998

70. Studies investigating the effects of high-doses (>625 mg) of
aspirin and its derivative acetylsalicylic acid on human
periodontal diseases have demonstrated that people taking
aspirin had reduced plaque and gingival indices, probing
depth and attachment loss
Waite et al. 1981, Feldman et al. 1983, Flemmig et al. 1996

71. CONCLUSION: Systemic administration of Clopidogrel for 3 days
improved the repair process associated with experimental periodontal
disease, suggesting that it may have therapeutic value under situations
where tissues undergo a transition from inflammation to repair.

72. AIM: This study investigated the periodontal status of non-smokers and ex-
smokers in relation to their intake of low-dose aspirin
CONCLUSION: individuals aged over 50 years, particularly ex-smokers, may
benefit by taking low-doses of aspirin daily to reduce their risk of periodontal
attachment loss.

73. PROPIONIC ACID DERIVATIVE:
IBUPROFEN
• Discovered by Dr. Stewart Adams and his colleagues in the
United Kingdom in the 1950s, patented in 1961
• Ibuprofen was the first member of this class, 1969
• Better tolerated alternative to aspirin
• Analgesic, antipyretic & anti-inflammatory efficacy is
lower than Aspirin
• Most potent: Naproxen
• Inhibition of platelet aggregation is short lasting

74. USES
• ‘over the counter’ drug as analgesic and antipyretic.
• Rheumatoid arthritis, osteoarthritis , other musculoskeletal
disorders specially when pain is more prominent than
inflammation
• Soft tissue injury, tooth extraction, fractures, vasectomy, post
partum and post operatively : supress swelling and
inflammation
• VERY POPULAR IN DENTISTRY

75. ADVERSE EFFECTS
• Most common: nausea, gastric discomfort and vomiting (less
than aspirin or indomethacin)
• Gastric erosion and occult blood loss-rare
• CNS: headache, dizziness, blurring of vision, tinnitus,
depression
• Rashes, itching and other hypersensitivity phenomenon are
infrequent
CONTRAINDICATED in pregnant woman and peptic ulcer patient

76. PHARMACOKINETICS &
INTERACTIONS
• Well absorbed orally
• 90-99% bound to plasma proteins
• Enter brain, synovial fluid & cross placenta
• Metabolized in liver
• Excreted in urine as well as bile
Because they interact with platelet function, SHOULD NEVER BE USED
with anticoagulants

77. DRUG PLASMA
t1/2
DOSAGE PREPERATIONS
1 IBUPROFEN 2 hr 400-600mg(5-
10mg/kg) TDS
BRUFEN,EMFLAM,
IBUSYNTH
200,400,600 mg
T,IBUGESIC also
100mg/5ml
suspension
2 NAPROXEN 12-16hr 250mg BD-
TDS
NAPROSYN,NAXID,
ARTAGEN,XENOBI
D 250mg
T,NAPROSYN also
500mg T
3 KETOPROFEN 2-3hr 50-100mg BD-
TDS
KETOFEN 50,100mg
T,OSTOFEN 50mg
C,RHOFENID
100mg,200mg SR T,
T,100mg/200ml amp
4 FLURBIPROFEN 4-6hr 50mg BD-QID ARFLUR 50,100mg
T,200mg SR
T,FLUROFEN

78. IBUPROFEN: rated as the safest conventional NSAID by
the spontaneous adverse drug reaction system in U.K.
IBUPROFEN: equally or more efficacious than a
combination of Aspirin (650 mg)+ Codeine (60 mg) in
relieving dental surgery pain
Cooper et al., 1977; Jain et al., 1986; Forbes et al., 1984

79. PERIODONTAL INDICATIONS
• Ibuprofen , because of its rapid onset of action and long duration, its
favourable safety profile and the possibility of easy oral administration
shortly before a dental procedure, is a promising agent to achieve pain
control during and after periodontal SRP
Fornasini et al. 1997, Black et
al. 2002
• first demonstrated that beagles with naturally occurring periodontitis
treated with the NSAIDs, flurbiprofen (0.02 mg/kg) exhibited significant
depressions in GCF,PGE2 and concomitant decreases in alveolar bone
loss
Williams et
al. 1988
Recently documented of significant reductions in crevicular prostanoids
(PGE2 and LTB4) and alveolar bone loss in periodontally diseased monkeys
treated with topical 1.0% ketoprofen creams over a 6 month dosing period

80. AIM: the influence of short-term ibuprofen therapy on the early phase
of the treatment of adult chronic periodontitis
CONCLUSION: significantly greater reduction in gingival bleeding,
colour and pocketing was detected in the test compared with the
control group

81. AIM: to investigate the analgesic efficacy and tolerability of ibuprofen
arginine in patients with mild-to-moderate periodontitis during and after
non-surgical periodontal treatment
CONCLUSION: In patients with mild-to-moderate chronic periodontitis,
ibuprofen arginine was safe and superior for alleviating pain during non-
surgical periodontal treatment. Its painless administration and rapid onset
of action make it well suitable for pain management in a general dental
office

82. ANTHRANILIC ACID DERIVATIVE:
MEPHENAMIC ACID
It is an analgesic, antipyretic and weaker antiinflammatory
agent, which inhibits COX as well as antagonises certain
actions of PGs.
Mephenamic acid exerts peripheral as well as central
analgesic action.
ADVERSE EFFECTS
Diarrhoea is the most important dose related side effect
Haemolytic anaemia: rare

83. PHARMACOKINETICS
Oral absorption is slow but almost complete.
It is highly bound to plasma proteins.
Partly metabolized and excreted in urine as well as bile.
Plasma t ½ is 2-4 hours.

84. USES
It is indicated as analgesic in muscle, joint and soft tissue
pain
It effective in dysmenorrhoea.
It may be useful in cases of rheumatoid and osteoarthritis.
DOSE
250-500mg TDS
MEDOL 250,500mg T
MEFTAL 250,500mg T;100mg/5ml susp.
PONSTAN 125,250,500mg T,50mg/ml syrup

85. AIM: to investigate the effect of NSAIDs to control postoperative pain after
periodontal surgery
RESULT: There was relatively equal pain control in group A and group B
according to VRS-4 and VAS.
CONCLUSION: Paracetamol in combination with ibuprofen and mefenamic
acid was equally efficient in the control of pain following a periodontal surgery

86. ARYL-ACETIC ACID DERIVATIVES
DICLOFENAC SODIUM
• Along with PG inhibition & is somewhat COX-2 selective, it
also reduces nutrophil chemotaxis
• Well absorbed orally; 99% protein bound
• Metabolized & excreted in urine & bile
• Plasma t1/2: 2 hrs
USE
• Toothache, Rheumatoid and osteoarthritis, bursitis,
ankylosing spondylitis, dysmenorrhoea, post traumatic and
post operative inflammatory conditions  affords quick relief
of pain and wound oedma.

87. DOSE
• 50mg TDS, then BD oral, 75mg deep im
• VOVERAN, DICLONAC, MOVONAC 50mg enteric coated
T,100mg SRT,25mg/ml in 3ml amp for im inj.
• Diclofenac potassium: VOLTAFLAM 25, 50 mg T,
• VOVERAN 1% topical gel.
ACECLOFENAC
• relatively selective COX2 congener of diclofenac sodium
DOSE
• Dose : 100mg BD
• ACECLO,DOLOKIND 100mg T,200 mg SRT.

88. ADVERSE EFFECTS
• Epigastric pain
• Nausea
• Headache
• Dizziness
• Rashes
• Gastric ulceration & bleeding are less common
• Reversible increase in serum aminotransferases
• Kidney damage is rare.

89. CONCLUSION: Diclofenac sodium seemed to delay peri-implant bone
healing and to decrease BIC, whereas meloxicam had no negative effect
on peri-implant bone healing.

90. AIM: to evaluate the effect of Diclofenac mouthwash on periodontal
postoperative pain
CONCLUSION: Diclofenac mouthwash was effective in reducing
postoperative periodontal pain but it seems that it isn’t enough to control
postoperative pain on its own.

91. OXICAM DERIVATIVES:
PIROXICAM
• Long acting, potent NSAID with good antiinflammatory action.
MOA
• Reversible inhibitor of COX.
• Lowers concentration of PG in synovial fluid & inhibits platelet aggregation
• Decreases production of IgM Rheumatoid factor.
• Chemotaxis of leucocytes is inhibited.
PHARMACOKINETICS
• Well absorbed orally, 99% is plasma bound, metabolized in liver
• T1/2 : 2days
• Single daily dose is sufficient.

92. ADVERSE EFFECTS
• Heartburn, nausea, anorexia are common
• Better tolerated and less ulcerogenic
• Cause less faecal blood loss than aspirin
• Rashes and pruritis are seen in < 1 % cases
• Edema and reversible
USES
• Piroxicam – short term analgesic and long term antiinflammatory
drug in Rhematoid and osteoarthritis, ankylosing spondylitis, acute
gout, musculoskeletal injuries and in dentistry.

93. DOSE
• 20 mg BD for 2 days followed by 20mg OD
• DOLONEX,PIROX 10,20 mg Cap , 20mg disp Tab, 20mg/ml
inj in 1 and 2 ml amp
• PIRICAM 10,20 mg Cap

94. PERIODONTAL INDICATIONS
• A Cochrane review has shown that piroxicam has an efficacy
similar to that of other NSAIDs and of intramuscular
morphine (10 mg), when used as a single oral dose in the
treatment of moderate to severe postoperative pain, thus
representing an alternative to other analgesics in various pain
states
Piroxicam penetrates inflamed tissues easily, has extended
plasma half life and minimal liver & kidney load. This factor
make it an excellent candidate for local delivery for oral
inflammatory disease

95. In this study, patients undergoing oral surgery were treated with piroxicam
and azithromycin to examine the interactions of these drugs on periodontal
tissues
CONCLUSION: Treatment with piroxicam or azithromycin alone ensures a
favorable distribution of these drugs into periodontal tissues. However, upon
combined administration, azithromycin interferes negatively with the
periodontal disposition of piroxicam. This interaction might depend on the
displacement of piroxicam from acceptor sites at the level of periodontal
tissues.

96. AIM: to study the effects of piroxicam in preventing gingival inflammation and
plaque formation in beagle dogs.
RESULT: By week 2, the gingival index in the piroxicam-treated dogs was
significantly lower than that of the placebo-treated group and remained so
throughout the study, with the exception of wk 6 and 12 in the topical gel-
treated group. Mean percent bleeding sites were also significantly less in the
piroxicam-treated groups than in the control dogs.
CONCLUSION: piroxicam can significantly inhibit the development of
gingival inflammation in beagle dogs.

97. PYROLLO-PYROLLE
DERIVATIVES: KETOROLAC
• Novel NSAID with potent analgesic, modest anti inflammatory
activity.
• In post operative pain it has equaled efficacy of Morphine but do
not have morphine like side effects.
USES
1. Post operative ,dental pain & Acute musculoskeletal pain (15-
30mg im or iv)
2. Renal colic
3. Migraine
4. Pain due to bony metastasis.

98. • Continuous use for more than 5 days is not recommended
• Should not be given to patients on oral anticoagulants.
• Not indicated for preanaesthetic medication or for obstetric
analgesia.
• Cause Dizziness, Dyspepsia, Nausea and pain at site of injection
DOSES
• KETOROL, ZOROVON, KETANOV, TOROLAC 10mg Tab, 30mg in
1 ml amp

99. AIM: to evaluate the analgesic efficacy of preoperative ketorolac
tromethamine administration on periodontal postoperative pain
RESULT: preoperative treatment with ketorolac significantly reduced
initial pain intensity and delayed the onset of postoperative pain as
compared to placebo.

100. INDOLE DERIVATIVES:
INDOMETHACIN
It is a potent anti-inflammatory with prompt antipyretic
action
It relives only inflammatory or tissue related pain.
It is highly potent inhibitor of PG synthesis and suppresses
neutrophil motility.
PHARMACOKINETICS
It is well absorbed orally, rectal absorption is slow but
dependable.
It is 90% bound to plasma proteins, partly metabolized in
liver to inactivate products and excreted by kidney.
Plasma t1/2 is 2-5 hours.

101. ADVERSE EFFECTS
A high incidence of gastrointestinal and CNS side effects is
produced
Increased risk of bleeding due to decreased platelet aggregation
Leucopenia ,rashes and other hypersensitivity reactions are also
reported

102. USES
Rheumatoid arthritis
Ankylosing spondylitis
Acute exacerbations of destructive artropathies
Psoriatic arthritis
Acute gout
Closure of patent ductus arteiosus dose; 0.1-0.2 mg/kg
DOSE
25-50 mg BD-QID
INDICIN, INDOCAP 25mg C,75mg SR C, ARTICID
25,50mg C,INDOFLAM 25,75mg C,1% eye drop

103. PERIODONTAL INDICATION
NSAIDs such as “Indomethacin”, administered daily for
upto 3 years significantly slowed the rate of alveolar bone
loss

104. AIM: The effect of two non-steroidal anti-inflammatory drugs,
indomethacin and flurbiprofen, on the progression of periodontal disease
was studied in 16 beagle dogs over a 12-month period.
CONCLUSION: both flurbiprofen and indomethacin inhibit alveolar bone
loss in beagles compared to untreated controls.

105. PYRAZOLONE
• ANTIPYRINE AND AMIDOPYRINE were introduced in
1884 as antipyretics and analgesics.
• Their use was associated with agranulocytosis
• PHENYLBUTAZONE was introduced in 1949 but are
rarely used now due to risk of bone marrow depression.
• Two other pyrazolone-METAMIZOL and
PROPIPHENAZONE: used as analgesic &
antipyretic

106. METAMIZOL (DIPYRONE)
• It is a derivative of amidopyrine which continues to be
widely used.
• In contrast to phenylbutazone, it is a potent and promptly
acting analgesic & antipyretic but poor antiinflammatory
• It can be given orally, I.M. as well as I.V but gastric
irritation and pain at injection site occurs.

107. • Few cases of agranulocytosis were reported and Metemizol
was banned in USA.
• It has been extensively used in India and some European
countries.
DOSE
• 0.5-1.5 g oral/i.m/i.v
• ANALGIN 0.5g tab
• NOVALGIN, BARALGAN 0.5g tab,0.5gm/ml in 2ml and 5ml
amps,ULTRAGIN 0.5gm/ml inj in 2ml amp and 30ml vial

108. PROPIPHENAZONE
• Another pyrazolone, similar in properties to metamizol ; claimed
to be better tolerated.
• Agranulocytosis has not been reported
DOSE
• 300-600 mg TDS
• SARIDON,ANAFEBRIN : Propiphenazone 150 mg +
Paracetamol 250 mg.
• DART : propiphenazone 150mg + paracetamol 300mg + caffeine
50mg T.

109. PREFERENTIAL COX-2 INHIBITORS
NIMESULIDE
• Weak inhibitor of PG synthesis.
• Antiinflammatory action may be exerted by other mechanisms
like reduced generation of superoxide by nutrophils, inhibition
of PAF synthesis & TNF release, free radical scavenging,
inhibition of metalloproteinase activity in cartilage.
USES
• short lasting inflammatory conditions like sports injuries,
sinusitis, other ENT disorders, dental surgery, bursitis, low
back ache, dysmmenorrhea, post operative pain, osteoarthritis
and fever

110. PHARMACOKINETICS
• Completely absorbed orally
• 99% plasma protein bound
• Extensively metabolized and excreted mainly in urine
• Plasma t1/2: 2-5hrs

111. ADVERSE EFFECT
• GI: epigastralgia, heart burn, nausea, loose motion
• Dermatological: rashes, pruritis
• Central: dizziness
• Haematuria in children.
Recently several instances of fulminant hepatic failure have been
associated and hence banned in Spain, Finland, & Turkey and not
marketed in UK, USA, Australia, Canada

112. • Used in asthmatics who cannot tolerate ASPIRIN.
DOSE :
• 100mg BD; NIMULID,NIMEGESIC,NIMODOL,100mg
Tab, 50mg/ml susp
MELOXICAM
• newer congener of piroxicam
• has COX2/COX1 selectivity ratio 10
• Since measurable inhibition of platelet TXA2 occurs at
therapeutuc dose it has been labelled pref.COX2
DOSE:
• 7.5-15mg OD,MELFLAM,MEL-OD,MUVIK,M-CAM
7.5mg,15mg Tab

113. Diclofenac sodium seemed to delay peri-implant bone healing and to
decrease BIC, whereas meloxicam had no negative effect on peri-
implant bone healing

114. AIM: to appraise the effectiveness of transmucosal drug delivery system
with meloxicam films and to identify its minimum effective dosage via
this route after periodontal flap surgery
RESULT: The postoperative pain control observed in Groups A and B was
found to be effective, and the patient comfort level was very satisfactory.
Whereas in Group C, it was found to be high in the first 3 h
postsurgically, after which adequate pain relief was seen.
CONCLUSION: Transmucosal delivery of meloxicam was found to be
effective and safe in postsurgical pain control of periodontal flap surgery.
The minimum effective dosage via this route for meloxicam was found to
be with 30 mg mucoadhesive film

115. SELECTIVE COX-2 INHIBITORS (COXIBS)
• Celecoxib, Etoricoxib, Parecoxib, Rofecoxib, Valdecoxib,
Lumiracoxib
• Directly targets COX-2
• Reduces the risk of peptic ulceration
• Increased risk of myocardial infarction and stroke
OTHER CONCERNS WITH SELECTIVE COX-2
INHIBITORS
1. Do not have broad range of efficacy as traditional
NSAIDs
2. COX-2 inhibition may delay ulcer healing
3. JG COX-2 is constitutive, its inhibition can cause salt &
H2O retention
Pedal edema, precipitation of CHF, & rise in BP
can occur in all COXIBS

116. CELECOXIB
• Exerts anti-inflammatory, analgesic, antipyretic actions with
low ulcerogenic potential.
• PAF in response to collage remained intact
• TXA2 level not reduced
• Tolerability better than traditional NSAIDs
• Abdominal pain, dyspepsia, mild diarrhoea, rashes, edema,
rise in BP
ETORICOXIB
• Highest COX-2 selectivity
• Suitable for once-a-day treatment of acute dental surgery
• Without affecting platelet function or damaging gastric
mucosa
• Dry mouth, apthous ulcer, taste disturbance, paresthesia

117. DOSES
• Celecoxib 100-200 mg BD
CELACT, REVIBRA, COLCIBRA
• Etoricoxib 60-120mg OD
ETODY,TOROCOXIA,ETOXIB,NUCOXIA,60, 90, 120mg Tab
• Parecoxib 40mg oral im/iv repeated after 6-12hrs
REVALDO,VALTO-P 40mg/vial inj,PAROXIB 40mg T

118. AIM: To investigate the effect of etoricoxib, a selective cyclooxygenase- 2
inhibitor, and indomethacin, a non-selective cyclooxygenase inhibitor, on
experimental periodontitis, and compared their gastrointestinal side effects
RESULT: Histopathology of periodontium showed that etoricoxib and
indomethacin reduced inflammatory cell infiltration, ABL, and cementum
and collagen fiber destruction. Macroscopic and histopathological analysis of
gastric and intestinal mucosa demonstrated that etoricoxib induces less
damage than indomethacin. Animals that received indomethacin presented
weight loss starting on the 7th day, and higher mortality rate (58.3%)
compared to etoricoxib (0%).
CONCLUSION: Treatment with etoricoxib, even starting when ABL is
detected, reduces inflammation and cementum and bone resorption, with
fewer gastrointestinal side effects.

119. AIM: study evaluates the efficacy of using etoricoxib and dexamethasone for
pain prevention after open-flap debridement surgery.
CONCLUSION: The adoption of a preemptive medication protocol using
either etoricoxib or dexamethasone may be considered effective for pain and
discomfort prevention after open-flap debridement surgeries.

120. PARA AMINO PHENOL DERIVATIVES
PHENACETIN
• Was introduced in 1887. It was extensively used but is now banned
in many countries because of analgesic abuse nephropathy
PARACETAMOL (ACETAMINOPHEN)
• The deethylated active metabolite of phenacetin but came into
common use since 1950.
• The central analgesic action of paracetamol is like aspirin
• Paracetamol is a good and promptly acting antipyretic
• Paracetamol is a poor inhibitor of PG synthesis in peripheral
tissues, but more active on COX in brain (poor ability to inhibit COX
in presence of peroxides generated at site of inflammation)
• Gastric irritation is insignificant; Mucosal erosion and bleeding occur
rarely only in overdose
• It does not affect platelet function or clotting factors.

121. PHARMACOKINETICS
• Well absorbed orally
• only 1/4th is plasma bound
• uniform distribution in body
• T1/2: 2-3hrs
• effect of an oral dose lasts for 3-5hrs

122. ADVERSE EFFECT
• Nausea and rashes are occasional
• Leukopenia is rare
• Acetaminophen overdose can cause hepatotoxicity, severe
hepatotoxicity has been reported even after therapeutic doses
• ANALGESIC NEPHROPATHY: occurs after years of heavy
ingestion of analgesics; such persons have some personality
defect

123. ACUTE PARACETAMOL POISONING
• Occurs specially in small children who have low hepatic
glucuronide conjugating ability
• If large dose is taken (>150mg/kg or >10g in an adult) serious
toxicity can occur ; fatality common with >250mg/kg
• Early manifestation : nausea, vomiting, abdominal pain, liver
tenderness, with no impairment of consciousness
• After 12-18hrs: hepatic necrosis renal tubular necrosis
hypoglycemia coma
• After 2 days: jaundice
• Further fulminating hepatic failure and death

124. MECHANISM OF TOXICITY
N-acetyl-p-
benzoquinoneimin
e (NABQI)
•Detoxified by
conjugation with
glutathione
Glucoronidation
capacity is
saturated
•More minor
metabolite is
formed
Hepatic
glutathione is
depleted
•Metabolites bind
covalently to
protein in liver
cells
necrosis
Paracetamol should
be avoided in chronic
alcoholics

125. TREATMENT
• If patient is brought early: vomiting is induced, gastric
lavage done, activated charcoal given to prevent further
absorption
• ANTIDOTE : N-acetylcysteine infused, 150 mg/kg i.v over 15
min followed by same dose for next 20 hrs.
• It replenishes the glutathione stores of liver & prevents
binding of toxic metabolite to the other cellular constituents
• Ingestion treatment is ineffective if started 16 hrs after
paracetamol ingestion
• Paracetamol is not recommended in premature infants for
fear of hepatotoxicity

126. USES
• Headache
• Musculoskeletal pain
• Toothache
• Dysmenorrhea
• Pregnant women & lactating mothers
• Much safer than aspirin in terms of GI manifestations
• Does not prolong bleeding time ; so less chance of post extraction
haemorrhage
• Can be used in all age groups

127. DOSE
• 0.5- 1g TDS
• infants 50mg
• children 1-3yrs 80-160mg
• 4-8yrs 240-320mg
• 9-12yrs 300-600mg
• CROCIN 0.5,1.0mg T, METACIN, PARACIN 500mg T
125mg/5ml syrup, 150mg/ml paed.drops
• ULTRAGIN,PYRIGESIC,CALPOL 500mg T,125mg/5ml
syrup
• NEOMOL,FEVASTIN,FEBRINIL 300mg/2 ml inj
• CROCIN PAIN RELIEF: paracetamol 650mg+caffeine 50mg
T

128. This study compared an alternative combination of acetaminophen, 500 mg,
with caffeine, 30 mg, to ibuprofen, 400 mg, in pain management after
periodontal surgeries.
CONCLUSION: Acetaminophen, 500 mg, with caffeine, 30 mg, can be used
efficiently in controlling postoperative pain after open flap debridement,
especially in patients with gastric ulcers or bleeding tendency because
acetaminophen is less hazardous than ibuprofen

129. CHOICE OF NSAIDS
1. Mild to moderate pain with little inflammation paracetamol or
low dose ibuprofen.
2. Acute musculoskeletal, osteoarthritic, injury associated
inflammation-a propionic acid derivative, diclofenac or coxib.
3. Postextraction or other acute short lasting pain-ketorolac,
diclofenac, nimesulide,a propionic acid derivative
4.Gastric intolerence to conventional NSAIDs-etoricoxib,
paracetamol
5. h/o asthma, anaphylactic reaction to aspirin or other NSAIDs-
nimesulide,COX2 inhibitor
6. Pregnancy-paracetamol best preferred, second best low dose
aspirin
7. Paediatric- paracetamol ,aspirin, ibuprofen, naproxen

130. DISADVANTAGES
• Administration for extended periods is necessary for
periodontal benefits to become apparent, and are associated
with significant side effects:
• gastrointestinal problems,
• hemorrhage (from decreased platelet aggregation),
• and renal and hepatic impairment.
• Research shows that the periodontal benefits of taking long-
term NSAIDs are lost when patients stop taking the drugs,
with a return to or even an acceleration of the rate of bone
loss seen before NSAID therapy, often referred to as a
“rebound effect” William RC j dent res 1991

131. • Inhibition of COX-1 by nonselective NSAIDs causes side
effects
• gastrointestinal ulceration and impaired hemostasis.
Use of selective COX-2 inhibitors reduce periodontal
inflammation without the side effects typically observed after
long-term (nonselective) NSAID
• Selective COX-2 inhibitors slowed alveolar bone loss in
animal models (Bezerra MM J Periodontol 1993) and
modified prostaglandin production in human periodontal
tissues (Vardar S J Periodontol 2003)

132. Author Purpose Host M
Agent
Parameters Subjects Results
Ishihara y,
nishihara t
et al
(1991)
demonstrate the
lipopolysaccharide
isolated from a.a
comitans strain
induced bone
resorption
Indomethacin
dexamethasone
PGE2 and IL-1
levels
Mouse PGE2 and IL-1
participate in LPS
induced bone
resorption in vitro.
Howell th,
fiorellini i,
weber hp et
al (1991)
To study the effects of
piroxicam in
preventing gingival
inflammation
and plaque formation
Piroxicam Gingival
inflammation
plaque index
Beagle dogs Significantly inhibit
the development of
gingival
inflammation
Roy S,
Feldman,
Szeto B et al
(1983)
To evaluate the effect
on bone
resorption: A
retrospective study
Aspirin (asp) or
aspirin plus
indomethcin
Radiographs Humans Percentage bone loss
for the entire
dentition was lower
in
asp group
Offenbacher
S, Odle BM
et al (1989)
metabolites of
cyclooxygenase
(co) during the
progression of
periodontitis
Flurbiprofen Crevicular fluid
levels of PGE2
and TXB2
Rhesus monkey prevented rise in
TXB2, but did not
affect increase in
PGE2.
Heasman
PA, et al
(1993)
efficacy of
flurbiprofen (50mg) on
both
developing and
established
gingivitis
Flurbiprofen GCF
concentration
of PGE2, TXB2
and LTB4,
Bleeding index
Human control gingival
inflammation with
both
preventive and
therapeutic
properties

133. RISK VERSUS BENEFITS OF NSAIDS
FOR PERIODONTAL DISEASE
TREATMENT
• NSAIDs - harmful side effects
• Gastrointestinal upset
• Haemorrhage
• Renal and hepatic impairment
• Induction of aseptic meningitis in previously healthy patients.
• Ibuprofen in high doses impairs wound healing
Proper et al,
1988
• It is not clear whether NSAIDs promote or hinder the overall
mineralization process in contemporary periodontal
regenerative therapy McAllister et al,

134. NSAID’S – ENZYMES COMBINATIONS
• Enzyme combination of NSAIDs helps in reduction of unwanted
drug effects while maintaining the anti-inflammatory/analgesic
efficacy.
• Protease enzymes belonging to family metalloprotease, have been
successfully tested for their antiinflammatory properties, which
include trypsin, chymotrypsin and serratiopeptidse
Miyata et al., 1971; McQuade and Crewther, 1969; Lyerly and Kreger,
1981; Aiyappa and Harris, 1976; Decedue et al 1979
• Proteolytic enzymes are large protein molecules and they will be
absorbed in an active form from GIT. To overcome their destruction
in stomach by hydrolysis, these tablets are given in enteric coated
dosage form and in combinations.

135. COMMERCIALLY AVAILABLE
COMBINATIONS
• Aceclofenac+Paracetamol+Serratiopeptidase- Acecloren,
Acekem-SP
• Diclofenac Potassium+Serratiopeptidase- Acfast d, Aldase D
(50mg)
• Diclofenac Sodium+Serratiopeptidase- Actimol S, Alnec -S
• Diclofenac Potassium+Chymotrypsin- Alfapsin-D, Alzibit-D
• Diclofenac Potassium+Trypsin+Chymotripsin- Chemofast-D,
Chymobel Plus
• Diclofenac Potassium+Trypsin

136. WHAT’S NEW ?
• NO-releasing nonsteroidal antiinflammatory drugs (NO-NSAIDs)
are a recently described class of NSAID derivatives generated by
adding a nitroxybutyl moiety through an short chain ester linkage
to the parental NSAID Elliott, McKnight, Cirino,J. L.
Wallace. 1995
• These compounds exhibit a markedly reduced gastrointestinal
toxicity, while retaining the antiinflammatory and antipyretic
activity of parent NSAID.

137. • Although NO-NSAIDs spare the gastric mucosa, they inhibit
prostaglandin generation and exert powerful antiapoptotic
and antiinflammatory effects.
• Preliminary animal studies indicate that NO-NSAIDs are
more effective than conventional NSAIDs in reducing
inflammation and pain in arthritic rats
Fiorucci,Antonelli, Santucci, O. Morelli, M. Miglietti, B.
Federici,A. Morelli. 1999

138. CONCLUSION
• Analgesics are definitely useful in reducing pain & improving
the quality of life but have their own spectrum of adverse
effects.
• No single drug is superior to all others for every patient.
Choice of drug is inescapably empirical.
“A GOOD LAUGH OR AT LEAST A BIG SMILE IS A
BODY’S NATURAL PAIN KILLER”

139. REFERENCES
 Essentials of pharmacology for dentistry; K D Tripathi – 2nd edition.
 Newman, Takei, Klokkevold, Carranza. Carranza’s clinical
periodontology; 11th edition
 Emanuela Ricciotti and Garret A. FitzGerald; Prostaglandins and
Inflammation; Arterioscler Thromb Vasc Biol . 2011 May ; 31(5): 986–
1000
 Daniel A. Haas; An Update on Analgesics for the Management of Acute
Postoperative Dental Pain; J Can Dent Assoc 2002; 68(8):476-82
 Tove Båge, Anna Kats, Blanca Silva Lopez, Gareth Morgan, Gunnar
Nilsson, Idil Burt, Marina Korotkova, Lisa Corbett, Alan J. Knox,
Leonardo Pino, Per-Johan Jakobsson, Thomas Modéer, and Tülay Yucel-
Lindberg; Expression of Prostaglandin E Synthases in Periodontitis
Immunolocalization and Cellular Regulation; The American Journal of
Pathology, Vol. 178, No. 4, April 2011

140. Dr. Prabhu MN; analgesics used in periodontal surgery;
International Journal of Innovations in Dental Sciences /
December 2016 / Vol 1 / Issue 1
M. Srinivas, Sangeetha Medaiah, S. Girish, M. Anil, Jagadish
Pai, Amit Walvekar; The effect of ketoprofen in chronic
periodontitis: A clinical double-blind study ; Journal of Indian
Society of Periodontology - Vol 15, Issue 3, Jul-Sep 2011
Drouganis A, Hirsch R; Low-dose aspirin therapy and
periodontal attachment loss in ex- and non-smokers. J Clin
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